Atelectasis and ARDS

Question 1

What is the definition of atelectasis

Answer 1

state at which the lung in whole or in part is **collapsed **or without air: loss of lung volume d/t inadequate expansion of airspaces

Question 2

What are the four types of atelectasis?

Answer 2

Resorption

compression

loss of surfactant

contraction

Question 3

In Resorption atelectasis, what is the consequence of complete airway obstruction?

Answer 3

stops air reaching alveoli

get resoprtion of air trapped in distal airspaces via pores of Kohn

lack of air in distal airspaces adn collapse

Question 4

In resoprtion atelectasis, where does obstruction occur?

Answer 4

bronchi, subsegmental bronchi or bronchioles

Question 5

What are some causes of obstruction in resorption atelectasis?

Answer 5

Mucus plug, following surgery

aspiration of foreign material

bronchial asthma/bronchitis/bronchiectasis

Bronchial neoplasmas

Question 6

What is the commenest cause of fever 24-36 hrs following surgery?

Answer 6

resoprtion atelectatis; see fever and dyspnea

Question 7

In Resorption atelectasis we see _____deviation of trachea and _____diaphragmatic elevation

Answer 7

ipsilateral

ispilateral

Question 8

Breath sounds and tactile fremitus increase/decrease/are absent in resorption atelectasis

Answer 8

both are absent

*collapsed lung doesn’t expand on inspiration

Question 9

Aor or fluid accumulation in pleural cavity–increased pressure–collapses underlying lung

Answer 9

Compression atelectasis

Question 10

tension pneumothorax and pelural effusion are both examples of

Answer 10

compression atelectasis

Question 11

in compression atelectass, the trachea and mediastinum shift ____ from the atelectatic lung

Answer 11

AWAY

Question 12

What do we notice about the lung in a patient with compression atelectasis?

Answer 12

lung field is hypertranslucent dt accumulation of air and collapse goesa way from collapsed lung

Question 13

What do we see on this HE of alveoli

Answer 13

collapsed alveoli with minimal white space

Question 14

In neonatal atelectasis, what causes collapse of alveoli?

Answer 14

loss of surfactant; especially issues with phosphatidlyglycerol

Question 15

Surfactant proteins A and D are responsible for _____

Surfactant proteins B and C are responsible for _____

Answer 15

innate immunity

reduction of surface tension at air liquid barrier in alveoli

Question 16

Surfactant is produced by _______ and begins at the ______ of gestation and stored in _______

Answer 16

produced by type 2 pneumocytes

synthesis begins by 28th week

stored in lamellar bodies

Question 17

Synthesis is modulated by different hormones

____ and ____ Increase production

_____decreases production

Answer 17

cortisol and thyroxine increase

insulin decreaes

Question 18

RDS in newborns is from decreased surfactant in fetal lungs, it can be a result of:

Answer 18

prematurity

maternal diabetes = increaesd insulin = decreased surfactant production

Cesarean section; labor + vaginal delivery increases stress related cortisol secreation adn increases surfactant production

Question 19

Collapsed alveoli are lined with

Answer 19

hyaline membrane

Question 20

In neonatal atelectasis, we see respiratory distress within in a few hours, see ________ and _______

What do we see on xray?

Answer 20

hypoxemia and respiratory acidosis

ground glass apperance

Question 21

What complications arrive from neonatal atelectasis?

Answer 21

intraventricular hemorrhage

patent ductuas arteriosus (persistant hypoxemia)

hyoglycemia (excessive insulin release)

O2 therapy-damage to lungs and cataracts

Question 22

in a premature infant, we see decreaed alveolar surfactant which leads to increaed alveolar tension and atelectasis which leads to:

Answer 22

uneven perfusion and hypoventilation

leads to acidosis

Question 23

See fibrotic atelectasis in lung or pleura prevents full expansion, this is not reversible. What kind of atelectasis is this?

Answer 23

contraction atelectasis

Question 24

Acute lung injury can be to what areas of lung>

Answer 24

endothelial and epithelial

Question 25

Acute lung injury can be heritable and non heritable and is mediated by:

Answer 25

cytokines, oxidants, growth factors; TNF, IL-1, 6 and 10 adn TGF-Beta

Question 26

What are the different manifestations we see from acute lung injury?

Answer 26

pulmnary edema, diffuse alveolar damage (ARDS)

Question 27

Pulmonary edema is edema due to:

Answer 27

alterations in Starling pressure

we have increased hydrostatic pressure in pulmonary capillaries

Decreased oncotic pressure

Transudate

Edema fluid accumulation in alveoli w/ heart fail cells adn brown induration

Question 28

In acute lung injury we see incrased hydrostatic pressure in pulmonary capillaries which causes:

Answer 28

left sided heart failure, volume overload, mitral stenosis and hemodynamic disturbances–cardiogenic pulmonary edema

Question 29

In acute lung indury decreased oncotic pressure leads to

Answer 29

nephrogenic syndrome, liver cirrhosis

Question 30

In acute lung injury, we see micovascular or alveolar injury to increase capillary permeability… what are those causes?

Answer 30

infection, aspiration, drugs, shock or traum and high altitude

Question 31

whats going on in these cells?

Answer 31

Hemosiderin laden macrophages = heart fail cells from acute lung injury and edema

Question 32

ARDS is alveolar injury, we get noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage; results in:

Answer 32

direct lung injury and indirect lung injury

Question 33

What are the big risks for noncardiogenic pulmonary edema, results from

Answer 33

Gram negative sepsis (40%)

Aspiration (30%)

Severe trauma (10%)

pulmonary infections

Question 34

Sepsis, diffuse lung infection, gastric aspiration adn physical injury are conditions assoicated with

Answer 34

ARDS

Question 35

What clincal findings do se wee in ARDS?

Answer 35

dysnpea, severe hypoxemia, NOT responsive to O2 therapy and respiratory acidosis

Question 36

In ARDS we see acute injury to epi or endo cell and alveolar macrophages release cytokines, this results in

Answer 36

neutrophil chemotaxsis, transmigration of neutrophils from caps into alveoli, leakage of protein(fibrin) exudate forming hyaline membrane and damage to pneumocytes–> causing low surfactant and atelectasis

Question 37

Prognosis of ARDS is poor with ____ mortality. This is due to

Answer 37

60% mortality

progresive interstital fibrosis

Question 38

What do we see on a cellular level in ARDS

Answer 38

sloughed bronchial epithelium

necrotic type I cell

edema fluid

cellular debris

hyaline membrane formation

neutrophil migration

Question 39

Days post injury: we see edema peak at day ___ in the ____ phase

Answer 39

1

exudative phase

Question 40

Hyaline membrane production peaks during day _____ and declines a few days later in the ____ phase

Answer 40

day 3, exudative phase

Question 41

Interstitial inflammation and interstitial fibrosis peak during what day and what phase?

Answer 41

day 10

proliferative phase